Viruses infect all life forms and each virus uses a unique approach to hijack its host cell and turn it into a virus replication factory. The virus that fascinates me, Epstein-Barr virus, infects people and causes cancers that are often fatal. Epstein-Barr virus has a remarkable relationship with people, often infecting infants and persisting within a person for life. During much of this time the virus enters a state of latency within cells and no virus replication occurs. However, once the lytic cycle is reactivated a cascade of viral gene expression ensues, the viral genome is replicated, and then virions are assembled and released, liberating hundreds of copies of virus from each cell. A long-term enigma that puzzled me about Epstein-Barr virus replication was whether the virus exploits some of the approximately 20,000 genes within the human cell to help its replication? Or whether it relies on its own genes and simply reuses the cellular contents as building blocks to generate new virus particles. Together with colleagues at the University of Sussex and collaborators at University College London, London Research Institute and the University of Birmingham, we recently used genome-wide technologies to discover that replication of Epstein-Barr virus causes the reprogramming of 2263 human genes. This provides a strong case in favor of the involvement of human genes in Epstein-Barr virus replication. Probing the mechanism of gene reprogramming identified a route for the regulation of a sub-set of the human genes – through the direct action of a viral protein. This specifically recognizes regions of DNA sometimes located at a gene start and sometimes located hundreds of thousands of nucleotides away. Research page @ASLAB